The optimal aerobic exercise training (AET) protocol for patients following myocardial infarction (MI) has remained under debate. The present study therefore aimed to compare the effects of continuous moderate-intensity training (CMT) and high-intensity interval training (HIT) on cardiac functional recovery, and to investigate the potential associated mechanisms in a post-MI rat model. Female Sprague Dawley rats (8-10 weeks old) undergoing MI or sham surgery were subsequently submitted to CMT or HIT, or kept sedentary for eight weeks. Prior to and following AET, echocardiographic parameters and exercise capacity of the rats were measured. Western blotting was used to evaluate the levels of apoptosis and associated signaling pathway protein expression. The concentrations of biomarkers of oxidative stress were also determined by ELISA assay. Messenger (m)RNA levels and activity of the key enzymes for glycolysis and fatty acid oxidation, as well as the rate of adenosine triphosphate (ATP) synthesis, were also measured. Compared with the MI group, exercise capacity and cardiac function were significantly improved following AET, particularly following HIT. Left ventricular ejection fraction and fraction shortening were further improved in the MI-HIT group in comparison to that of the MI-CMT group. The two forms of AET almost equally attenuated apoptosis of the post-infarction myocardium. CMT and HIT also alleviated oxidative stress by decreasing the concentration of malondialdehyde and increasing the concentration of superoxide dismutase and glutathione peroxidase (GPx). In particular, HIT induced a greater increase in the concentration of GPx than that of CMT. AET, and HIT in particular, significantly increased the levels of mRNA and the maximal activity of phosphofructokinase-1 and carnitine palmitoyl transferase-1, as well as the maximal ratio of ATP synthesis. In addition, compared with the MI group, the expression of signaling proteins PI3K, Akt, p38mapk and AMPK was significantly altered in the MI-CMT and MI-HIT groups. HIT was superior to CMT in its ability to improve cardiac function and exercise capability in a post-MI rat model. HIT was also superior to CMT with regard to attenuating oxidative stress and improving glucolipid metabolism of the post-MI myocardium.

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Glucagon-like peptide-1 (GLP-1) analogues might exert the cardioprotective effects via attenuating apoptosis. This study aimed to determine the protective effects and mechanism of exenatide, a GLP-1 analogue, on cardiomyocyte apoptosis using an in vitro model of hypoxia/reoxygenation (H/R). H9c2 cells were employed to establish an in vitro model of H/R. 200 nM exenatide pretreatment significantly reduced apoptosis measured by flow cytometry. To further study the antiapoptotic mechanism of exenatide, we used flow cytometry in combination with laser confocal microscopy to determine the interaction between exenatide and the process of mitochondria-mediated apoptosis. We found that exenatide pretreatment reduced the intracellular reactive oxygen species (ROS) levels and decreased the mitochondrial calcium overload caused by H/R. Furthermore, an increase of total superoxide dismutase (T-SOD) levels, a decrease of malondialdehyde (MDA) levels, a preservation of mitochondrial membrane potential (ΔΨm), a reduction of cytochrome-c release, a decline of cleaved caspase-3 expression, and caspase-3 activation were observed in exenatide-pretreated cultures. These results suggest that exenatide exerts a protective effect on preventing against H/R-induced apoptosis. Importantly, the protective effects of exenatide may be attributed to its role in improving mitochondrial function in H9c2 cells subjected to H/R.

BackgroundPrevious studies demonstrated conflicting results about the association of sleep duration and hypertension. Given the potential relationship between sleep quality and hypertension, this study aimed to investigate the interaction of self-reported sleep duration and sleep quality on hypertension prevalence in adult Chinese males.MethodsWe undertook a cross-sectional analysis of 4144 male subjects. Sleep duration were measured by self-reported average sleep time during the past month. Sleep quality was evaluated using the standard Pittsburgh Sleep Quality Index. Hypertension was defined as blood pressure level ≥140/90 mm Hg or current antihypertensive treatment. The association between hypertension prevalence, sleep duration, and sleep quality was analyzed using logistic regression after adjusting for basic cardiovascular characteristics.ResultsSleep duration shorter than 8 hours was found to be associated with increased hypertension, with odds ratios and 95% confidence intervals (CIs) of 1.25 (95% CI, 1.03–1.52) for 7 hours, 1.41 (95% CI, 1.14–1.73) for 6 hours, and 2.38 (95% CI, 1.81–3.11) for <6 hours. Using very good sleep quality as the reference, good, poor, and very poor sleep quality were associated with hypertension, with odds ratios of 1.20 (95% CI, 1.01–1.42), 1.67 (95% CI, 1.32–2.11), and 2.32 (95% CI, 1.67–3.21), respectively. More importantly, further investigation of the association of different combinations of sleep duration and quality in relation to hypertension indicated an additive interaction.ConclusionsThere is an additive interaction of poor sleep quality and short sleep duration on hypertension prevalence. More comprehensive measurement of sleep should be performed in future studies.

SUMMARY BackgroundThe association between meat consumption and the risk of hepatocellular carcinoma (HCC) is still inconclusive.